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 29 July 2016

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News

Non-redundant properties of interleukin during acute colon inflammation

The latest issue of Gut reports non-redundant properties of interleukin IL-1a and IL-1 during acute colon inflammation in mice.

News image

Dr Elena Voronov and colleagues from Israel studied the differential role of the IL-1 agonists, IL-1α, which is mainly cell-associated versus IL-1β, which is mostly secreted, in colon inflammation.

Dextran sodium sulfate (DSS) colitis was induced in mice globally deficient in either IL-1α or IL-1β, and in wild-type mice, or in mice with conditional deletion of IL-1α in intestinal epithelial cells.

The team performed bone marrow transplantation experiments to assess the role of IL-1α or IL-1β of myeloid versus colon non-hematopoietic cells in inflammation and repair in acute colitis.

IL-1α released from damaged intestinal epithelial cells acts as an alarmin by initiating and propagating colon inflammation, as IL-1α deficient mice exhibited mild disease symptoms with improved recovery.

The team found that IL-1β is involved in repair of intestinal epithelial cells and reconstitution of the epithelial barrier during the resolution of colitis.

The research team noted that its deficiency correlates with disease exacerbation.

Neutralization of IL-1α in control mice during acute colitis led to alleviation of clinical, and histological manifestations, whereas treatment with rIL-1Ra or anti-IL-1β antibodies was not effective.

The team found that repair after colitis correlated with accumulation of CD8, and regulatory T cells in damaged crypts.

Dr Voronov and team comments, "The role of IL-1α and IL-1β differs in DSS-induced colitis in that IL-1α, mainly of colon epithelial cells is inflammatory, whereas IL-1β, mainly of myeloid cell origin, promotes healing and repair."

"Given the dissimilar functions of each IL-1 agonistic molecule, an IL-1 receptor blockade would not be as therapeutically effective as specific neutralising of IL-1α, which leaves IL-1β function intact."

Gut 2014; 63: 598-609
17 March 2014

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